The experimental part (90%) of this study will examine the known neurotoxicity and the possible neuroteratogenicity of the vinyl monomer acrylamide and the ketonic solvent 2,5-hexanedione (the primary toxic metabolite of the hexacarbon solvents n-hexane and methyl n-butyl ketone). These compounds are widely used in commercially important polymers and solvents, but their neurotoxic properties make them significant industrial chemical hazards and environmental pollutants. Previous experimental studies with these chemicals, in which we demonstrated their ability to produce central-peripheral distal axonopathy, will be extended to examine by light and electron microscopy and by electron microprobe analysis: 1) the brain damage produced by chronic low-level systemic intoxication; 2) the extent and reversibility of nervous system damage after chronic exposure to these neurotoxins; 3) the differential effects of acute and chronic intoxication on the axon and supporting cells (Schwann cell, oligodendrocyte and astrocyte) in fetal, post-natal, adult, and aged states. These data will bear heavily on our understanding of the site of action of these agents and why the distal parts of central and peripheral nerve fibers are vulnerable to systemic intoxication. Light and electron microscopy will also be employed to study any abnormalities in the nervous system of fetal and post-natal rats which have been exposed to acrylamide or to 2,5-hexanedione in utero. The clinical part (10%) of this study will develop and evaluate a simple assay of palmar vibration sensibility presently being used in acrylamide manufacturing plants for the detection of early, sub-clinical neurological damage in potentially exposed workers. The objectives of these studies are 1) to meet some of the Research Needs specified in National Institute of Occupational Safety and Health Criteria documents for Acrylamide (1976) and Alkanes (1977) and elsewhere in U.S. Environment Protection Agency reports on Acrylamide (1976, 1977) and Diketone Solvents (1977), 2) to develop new, sensitive methods for the assessment of chemically induced neurotoxicity and neuroteratogenicity, and 3) to illuminate the mechanism of neurotoxin-induced nerve fiber degeneration.